European Research team in Algorithms and Biology, formaL and Experimental

Research themes

Parasitic protists include agents of human and animal diseases that have a huge impact on world populations and economy. The major public health problems of protozoan organisms come mainly from the phylum Apicomplexa or the Class Kinetoplastida (from the phylum Euglenozoa).

Worldwide, apicomplexans such as Plasmodium account for up to 500 million clinical cases of malaria each year, with up to 2 million deaths, while Toxoplasma gondii infects approximately one-third of the human population. Kinetoplastid diseases such as sleeping sickness, leishmaniases and Chagas disease are considered “neglected diseases of poverty”, afflicting millions of people and collectively responsible for over 150000 deaths per year. There are no vaccines, profilaxy or effective treatments available.

Although clearly distinct in many aspects, the members of the two groups bear many similarities. Phylogenetic studies have shown that they have diverged very early from other eukaryotes during the course of evolution. The nuclear transport for instance is an event that arose early in the evolution of eukaryotic cells, and is essential for the survival of the these parasitic protists. The latter do not possess a conserved machinery leading to the hypothesis that such parasites must have specific and unique factors. Thus, understanding these divergent characteristics can help elucidate the evolutionary history of key events. Also, both apicomplexans and kinetoplastids bear a single and unusually well developed mitochondrion. They undergo distinct morphological and physiological changes in the course of their complex life cycles, which means that the development of each stage has to be tightly controlled at both the transcriptional/post-transcriptional and translational/post-translational levels in order for these parasites to control major metabolic changes and be able to better communicate with their hosts. Recent studies have shown that some parasites are able to subvert the miRNAs of the host to its own benefit; but the question whether the host can also control its parasites through its miRNA machinery remains open.

An important subject yet largely under-explored is the fact that most members from these groups are pathogenic while a small fraction is not, which raises the question of what gives origin to the pathogenicity of these parasites. This is the main question we wish to address, by means of computational methods and wet-lab experiments, with the longer-term aim of trying to understand how to control it.

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